InVivoMAb anti-mouse Thy1.2 (CD90.2)
Product Description
Specifications
| Isotype | Rat IgG2b, κ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG2b isotype control, anti-keyhole limpet hemocyanin |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | Mouse thymus or spleen |
| Reported Applications |
in vivo ILC depletion in vivo T cell depletion Western blot |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
≤1EU/mg (≤0.001EU/μg) Determined by LAL assay |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Purification | Protein G |
| RRID | AB_1107682 |
| Molecular Weight | 150 kDa |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Application References
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Ermann, J., et al (2014). "Nod/Ripk2 signaling in dendritic cells activates IL-17A-secreting innate lymphoid cells and drives colitis in T-bet-/-.Rag2-/- (TRUC) mice" Proc Natl Acad Sci U S A 111(25): E2559-2566.
PubMed
T-bet(-/-).Rag2(-/-) (TRUC) mice spontaneously develop microbiota-driven, TNF-mediated large bowel inflammation that resembles human ulcerative colitis. We show here that IL-23 and IL-1-dependent secretion of IL-17A by innate lymphoid cells (ILCs; defined as CD45(+)lin(-)Thy1(hi)NKp46(-)) is a second critical pathway in this model. Using an in vitro coculture system of bone marrow-derived dendritic cells (DCs) and freshly isolated FACS-purified ILCs, we demonstrate that IL-23 and IL-1 secreted by DCs in response to microbial stimulation work together to induce IL-17A production by ILCs. TNF is not required for IL-17A secretion by ILCs in vitro but synergizes with IL-17A to induce the expression of neutrophil-attracting chemokines. Upstream, activation of the IL-23/IL-17A axis is regulated by nucleotide-binding oligomerization domain containing (Nod)/receptor-interacting serine-threonine kinase 2 (Ripk2) signals in DCs. Genetic ablation of the Nod/Ripk2 signaling pathway protects TRUC mice from developing colitis without affecting the colitogenicity of the intestinal microbiota. Our data provide insight into the complex network of interactions between IL-17A-secreting ILCs and other components of the innate immune system in the development of colitis.
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Gladiator, A., et al (2013). "Cutting edge: IL-17-secreting innate lymphoid cells are essential for host defense against fungal infection" J Immunol 190(2): 521-525.
PubMed
IL-17-mediated immunity has emerged as a crucial host defense mechanism against fungal infections. Although Th cells are generally thought to act as the major source of IL-17 in response to Candida albicans, we show that fungal control is mediated by IL-17-secreting innate lymphoid cells (ILCs) and not by Th17 cells. By using a mouse model of oropharyngeal candidiasis we found that IL-17A and IL-17F, which are both crucial for pathogen clearance, are produced promptly upon infection in an IL-23-dependent manner, and that ILCs in the oral mucosa are the main source for these cytokines. Ab-mediated depletion of ILCs in RAG1-deficient mice or ILC deficiency in retinoic acid-related orphan receptor c(-/-) mice resulted in a complete failure to control the infection. Taken together, our data uncover the cellular basis for the IL-23/IL-17 axis, which acts right at the onset of infection when it is most needed for fungal control and host protection.
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Brasseit, J., et al (2015). "CD4 T cells are required for both development and maintenance of disease in a new mouse model of reversible colitis" Mucosal Immunol. doi : 10.1038/mi.2015.93.
PubMed
Current therapies to treat inflammatory bowel diseases have limited efficacy, significant side effects, and often wane over time. Little is known about the cellular and molecular mechanisms operative in the process of mucosal healing from colitis. To study such events, we developed a new model of reversible colitis in which adoptive transfer of CD4+CD45RBhi T cells into Helicobacter typhlonius-colonized lymphopenic mice resulted in a rapid onset of colonic inflammation that was reversible through depletion of colitogenic T cells. Remission was associated with an improved clinical and histopathological score, reduced immune cell infiltration to the intestinal mucosa, altered intestinal gene expression profiles, regeneration of the colonic mucus layer, and the restoration of epithelial barrier integrity. Notably, colitogenic T cells were not only critical for induction of colitis but also for maintenance of disease. Depletion of colitogenic T cells resulted in a rapid drop in tumor necrosis factor alpha (TNFalpha) levels associated with reduced infiltration of inflammatory immune cells to sites of inflammation. Although neutralization of TNFalpha prevented the onset of colitis, anti-TNFalpha treatment of mice with established disease failed to resolve colonic inflammation. Collectively, this new model of reversible colitis provides an important research tool to study the dynamics of mucosal healing in chronic intestinal remitting-relapsing disorders.
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Monticelli, L. A., et al (2011). "Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus" Nat Immunol 12(11): 1045-1054.
PubMed
Innate lymphoid cells (ILCs), a heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor a-chain (CD25), IL-7 receptor a-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus.
Product Citations
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Long-term inhibition of protease hypersensitivity by initial immunological cross-regulation and epigenetic memory in lung stromal cells.
In Nat Immunol on 1 April 2026 by Ryu, J., Blondeau, A., et al.
PubMed
Prevention and regulation of excessive inflammation is a key target to protect against inflammatory pathologies such as autoimmunity and allergy. In a mouse model of acute lung protease hypersensitivity, we assessed the efficacy of immunological cross-regulation to mitigate pathogenic inflammation. We show that induction of a type 1 response using Toll-like receptor ligands or a bacterial lysate efficiently blocks acute eosinophilia and type 2 responses evoked by the cysteine protease papain. Upon rechallenge with papain weeks later, mice displayed enhanced type 2 responses and eosinophilia, whereas this response was absent if the initial inflammation was cross-regulated. Memory of the initial event was stored in adventitial stromal cells expressing CCL11. Accessibility of the Ccl11 locus was increased by papain exposure in an interleukin-4- and interleukin-13-dependent manner and blocked by interferon gamma. Our results show how the nature of an initial inflammation is memorized by tissue-resident cells and shapes subsequent inflammatory responses.
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Lung tissue-resident memory T cells optimize protection by IL-10 regulation of innate immunity.
In J Exp Med on 5 January 2026 by Yang, A. Y., Davis-Porada, J., et al.
PubMed
Respiratory viral infections establish tissue-resident memory T cells (TRM) in the lung, which provide optimal protection against subsequent infections, though the underlying mechanisms are incompletely understood. Here, we demonstrate in a mouse model of heterosubtypic influenza infection that lung TRM attenuate inflammation by macrophages during secondary versus primary responses, in part, through production of the immunoregulatory cytokine IL-10. During secondary infections, lung TRM were the predominant producers of early IL-10; inhibiting early IL-10 signaling resulted in increased macrophage-mediated inflammation, morbidity, and lung pathology. Moreover, lung TRM were shown to directly modulate lung macrophage responses and polarization in depletion experiments. Finally, IL-10 enhanced IFN-γ production by lung memory CD8+ T cells. Human influenza-specific TRM isolated from lungs recapitulated robust IL-10 expression associated with augmented effector responses of murine TRM. These data support a dual role of TRM in coordinating in situ secondary responses-augmenting effector responses for robust viral clearance while dampening inflammation to limit tissue damage.
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Complement-producing adventitial fibroblasts form an IL-33 alarmin hub that maintains ILC2s during airway allergy.
In Cell Rep on 23 December 2025 by Atakkatan, A., Magesh, A., et al.
PubMed
Once considered mere scaffolds, mesenchymal stromal cells are now recognized as actively shaping airway immunity. We identify adventitial fibroblasts (AFs) in perivascular/peribronchial cuffs as a dominant source of complement C3. At baseline, a discrete subset of AF co-expresses C3 and IL-33. Upon allergen exposure, these C3+IL-33+ AFs expand and increase their production of both C3 and IL-33, indicating a shift toward an allergic AF phenotype. Disruption of C3 production in AFs abrogates IL-33 expression, underscoring the essential role C3 plays in maintaining an allergic AF phenotype. Functionally, C3 from AFs is required to drive allergen-induced group 2 innate lymphoid cell (ILC2) responses. C3+ AFs not only support ILC2s but are also influenced by ILC2-derived IL-13, which, in turn, promotes AF function, perpetuating the allergic response. These findings reveal that aberrant C3 production by the adventitial stroma orchestrates a pathogenic AF-ILC2 niche that promotes allergic inflammation.
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LAMP2-FLOT2 interaction enhances autophagosome-lysosome fusion to protect the septic heart in response to ILC2.
In Autophagy on 1 September 2025 by Shao, R., Liu, W., et al.
PubMed
Cardiac dysfunction is a serious complication of sepsis-induced multiorgan failure in intensive care units and is characterized by an uncontrolled immune response to overwhelming infection. Type 2 innate lymphoid cells (ILC2s), as a part of the innate immune system, play a crucial role in the inflammatory process of heterogeneous cardiac disorders. However, the role of ILC2 in regulating sepsis-induced cardiac dysfunction and its underlying mechanism remain unknown. The present study demonstrated that autophagic flux blockage exacerbated inflammatory response and cardiac dysfunction, which was associated with mortality of sepsis. Using a cecal ligation and puncture (CLP) mouse sepsis model, we observed an expansion of ILC2s in the septic heart. Furthermore, IL4 derived from ILC2 mitigated cardiac inflammatory responses and improved cardiac function during sepsis. Additionally, IL4 enhanced LAMP2 (lysosomal associated membrane protein 2) expression through STAT3 (signal transducer and activator of transcription 3) activation to stabilize lysosomal homeostasis and rescue the impaired autophagic flux during sepsis. Notably, LAMP2 was preferentially bound to FLOT2 (flotillin 2) after IL4 exposure, and the interaction enhanced autophagosome-lysosome fusion in cardiac endothelial cells. Loss of FLOT2 reversed the regulatory effects of LAMP2 on autophagy mediated by IL4, leading to autophagosome accumulation and suppressed autophagosome clearance. Conclusively, these findings provide novel insights that ILC2 regulates incomplete autophagic flux to protect septic heart and expand our understanding of immunoregulation for sepsis.Abbreviation: ACTB: actin beta; ACTN: actinin, alpha; ADGRE1/F4/80: adhesion G protein-coupled receptor E1; ANXA5/annexin V: annexin A5; AO: acridine orange; BECN1/Beclin1: beclin 1, autophagy related; CKM: creatine kinase, muscle; CKB: creatine kinase, brain; CLP: cecal ligation and puncture; CO: cardiac output; CQ: chloroquine; CTS: cathepsin; DAPI: 4'6-diamidino-2-phenylindole; EC: endothelial cell; EF: ejection fraction; ELISA: enzyme-linked immunosorbent assay; FLOT: flotillin; FS: fractional shortening; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GATA3: GATA binding protein 3; GLB1/β-Gal: galactosidase, beta 1; HCMEC: human cardiac microvascular endothelial cell; IL: interleukin; ILC: innate lymphoid cell; IL1RL1/ST2: interleukin 1 receptor-like 1; IL4c: IL4 complex; IL7R/CD127: interleukin 7 receptor; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP: lysosomal-associated membrane protein; LDH: lactate dehydrogenase; LMP: lysosome membrane permeabilization; LPS: lipopolysaccharide; LVEDd: left ventricular end-diastole diameter; LVEDV: left ventricular end-diastole volume; LVESd: left ventricular end-systolic diameter; LVESV: left ventricular end-systole volume; MAN: mannosidase alpha; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MS: mass spectrometry; PECAM1/CD31: platelet/endothelial cell adhesion molecule 1; PTPRC/CD45: protein tyrosine phosphatase receptor type C; RORC/RORγt: RAR related orphan receptor gamma; SQSTM1/p62: sequestosome 1; TBX21/T-bet: T-box 21; TEM: transmission electron microscopy; THY1/CD90.2: thymus cell antigen 1, theta; TNF/TNF-α: tumor necrosis factor; V-ATPase: vacuolar-type H+-translocating ATPase; VIM: vimentin.